Secondary metabolites are low-molecular-weight organic compounds produced by plants under specific conditions. While they are not directly involved in fundamental growth and developmental processes, they play crucial roles in plant defense, protection, and regulation. These compounds mainly include phenolics, terpenoids, alkaloids, flavonoids, and others. Light, as a key environmental factor regulating the synthesis of plant secondary metabolites, influences their production and accumulation through multidimensional regulatory mechanisms. Different light qualities activate or suppress specific metabolic pathways via signal transduction networks mediated by specialized photoreceptors. Light intensity dynamically modulates secondary metabolite accumulation by affecting photosynthetic efficiency, while photoperiod coordinates metabolic rhythms through circadian clock genes. These light responsive mechanisms constitute a chemical defense strategy that enables plants to adapt to their environment, while also providing critical targets for the directed regulation of medicinal components and functional nutrients. This study provides a review of recent research on the effects of light on plant secondary metabolites, aiming to deepen the understanding of the molecular mechanisms underlying light-regulated secondary metabolism. The findings may offer an insight for enhancing bioactive compounds in medicinal plants and developing functional agricultural products.

Triple-negative breast cancer (TNBC) is a severe threat to women’s health because of its aggressive nature, early age of onset, and high recurrence rate. Therefore, in this study, we aimed to evaluate the anti-tumor effects of Gallic acid (GA) on the TNBC HCC1806 cells in vitro. The cell proliferation was detected by MTT and plate clone formation assays, cell apoptosis, cell cycle, and mitochondrial membrane potential (MMP) were analyzed by flow cytometry and Hoechst 33258 staining assays, and the intracellular reactive oxygen species (ROS) accumulation were also investigated. Real-Time PCR and western blot were examined to explore the mechanism of action. The results indicated that GA suppressed HCC1806 cells proliferation and promoted HCC1806 cells apoptosis. Meanwhile, GA treatment changed the morphology of the HCC1806 cells. In addition, GA blocked the HCC1806 cells cycle in the S phase, and it induced cells apoptosis accompanied by ROS accumulation and MMP depolarization. Real-Time PCR results suggested that GA increased Bax, Caspase-3, Caspase-9, P53, JINK and P38 mRNA expression, and decreased Bcl-2, PI3K, AKT and EGFR mRNA expression. Western blotting results suggested that GA increased Bax, cleaved-Caspase-3, cleaved-Caspase-9, P53, P-ERK1/2, P-JNK, P-P38 proteins expression, and decreased Bcl-2, P-PI3K, P-AKT, P-EGFR proteins expression. Furthermore, molecular docking suggested that GA has the high affinity for PI3K, AKT, EGFR, ERK1/2, JNK, and P38. In conclusion, GA could suppress HCC1806 cells proliferation and promote HCC1806 cells apoptosis through the mitochondrial apoptosis pathway and induces ROS generation which further inhibits PI3K/AKT/EGFR and activates MAPK signaling pathways. Our study will provide some new references for using GA in the treatment of TNBC.

Dendrobium officinale is an important edible and medicinal plant, with the Dendrobium officinale polysaccharide (DOP) being its primary active constituent, known for its diverse biological activities. In this study, DOP was extracted and characterized for its structural properties. The potential of DOP to ameliorate gastric ulcers (GUs) was investigated using an acetic-acid-induced GU model in rats. The results demonstrated that DOP exerted a multifaceted protective effect against GU, mitigating the deleterious impact on food intake and body weight in rats. DOP exhibited its protective action by attenuating cellular damage attributed to oxidative stress and inflammatory reactions mediated by enhanced activities of SOD, GSH, and GSH-PX, coupled with a downregulation in the expression of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. Furthermore, DOP effectively inhibited apoptosis in gastric mucosa cells of acetic-acid-induced GU rat models and facilitated the self-repair of damaged tissues. Remarkably, the DOP-200 and DOP-400 groups outperformed omeprazole in reducing the expression of IL-6 and malondialdehyde (MDA) in tissues, as well as IL-1β, IL-6, and TNF-α in serum. These groups also exhibited an improved expression of SOD in tissues and SOD, GSH, and GSH-PX in serum. A Western blot analysis of gastric mucosa demonstrated that the DOP-200 and DOP-400 groups significantly reduced the expression of NF-κBp65, phosphorylated NF-κBp65, FoxO3a, and Bim. The observed antagonism to GU appeared to be associated with the NF-κB cell pathway. Additionally, qRT-PCR results indicate that DOP reduced the mRNA transcription levels of IL-6, and TNF-α, which shows that the healing of GU is related to the reduction in the inflammatory reaction by DOP. However, the expression of EGF and VEGF decreased, suggesting that the mechanism of DOP inhibiting GU may not be directly related to EGF and VEGF, or there is an uncertain competitive relationship between them, so further research is needed.

Fever is caused by an increase in the heat production process when the body is under the action of a heat source or the dysfunction of the temperature center. Ellagic acid (EA) is a polyphenol dilactone that has anti-inflammatory, anti-tumor, and antioxidant activities. Male Sprague-Dawley rats were injected yeast to reproduce an experimental fever model (150 ± 20 g), and the rectal temperature and its change values were subsequently taken 19 h later; the excessive production of interleukin-1β (IL-1β) and prostaglandin2 (PGE2) induced by yeast was regulated to normal by EA administration. Rat brain metabolomics investigation of pyrexia and the antipyretic anti-inflammatory effect of EA was performed using Ultra-High-Performance Liquid Chromatography–Mass spectrometry (UPLC-MS). Twenty-six metabolites, as potential biomarkers, significantly altered metabolites that were found in pyretic rats, and eleven metabolites, as biomarkers of the antipyretic mechanism of EA, were significantly adjusted by EA to help relieve pyrexia, which was involved in glycerophospholipid metabolism and sphingolipid metabolism, etc. In conclusion, potential metabolic biomarkers in the brain shed light on the mechanism of EA’s antipyretic effects, mainly involving metabolic pathways, which may contribute to a further understanding of the therapeutic mechanisms of fever and therapeutic mechanism of EA.

Acute liver injury (ALI), which can progress to cirrhosis, hepatocellular carcinoma and acute liver failure, has become a global concern and a serious threat to human life and health. Isorhamnetin (ISO) is an O-methylated flavonol from the class of flavonoids. It has a protective effect on various organs, but its effect on ALI is still unclear in current studies. This study aimed to investigate the protective effect of ISO against D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced ALI and to explore the underlying molecular mechanisms. Ninety-six male Kunming mice were randomly divided into six groups and given the appropriate drug administration for 14 days. The ALI mouse model was established by intraperitoneal injection of 700 mg/kg D-GalN and 10 µg/kg LPS. Hematoxylin-eosin (HE) staining was performed to observe the histopathological changes. Enzyme-linked immunosorbent assay (ELISA) and quantitative Real-time Polymerase Chain Reaction (qRT-PCR) were performed to detect the expression of genes related to oxidative stress and inflammation. Inflammation and apoptosis related factors were detected by western blot. ISO alleviated D-GalN/LPS-induced ALI, reducing the alanine transaminase (ALT), aspartate transaminase (AST), and malondialdehyde (MDA) levels (P < 0.01), while improving histopathology (P < 0.05). Additionally, ISO elevated the superoxide dismutase (SOD) level, and improved the survival rate of mice (P < 0.01). Moreover, ISO reduced the nitric oxide (NO), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) levels (P < 0.05), while increasing the glutathione (GSH), and catalase (CAT) levels (P < 0.05). ISO also decreased the expression of nuclear factor-kappa B alpha (IκBα), Nuclear factor kappa-B (NF-κB) p65, IL-1β, IL-6, TNF-α, nitric oxide synthase (iNOS), and toll-like receptor 4 (TLR4) at the messenger ribonucleic acid (mRNA) level (P < 0.05). Furthermore, western blot showed that ISO decreased the expression of NF-κB p-p65, cysteine aspartate protease-3 (caspase-3), and B-cell lymphoma 2-associated X protein (Bax) proteins and elevated the expression of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma 2-like protein (Bcl-xL) proteins (P < 0.05). ISO could alleviate D-GalN/LPS-induced ALI by attenuating oxidative stress and inflammatory cytokines, enhancing the expression of anti-apoptotic proteins, reducing hepatocyte apoptosis, and inhibiting the activation of the NF-κB signaling pathway. Our study will provide some new references for treating ALI with ISO.